Publications

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2021
Martins, CF, Neves LA, Chagas R, Ferreira LM, Afonso CAM, Coelhoso IM, Crespo JG, Mota PBJ.  2021.  Modelling CO2 absorption in aqueous solutions of cholinium lysinate ionic liquid, OCT 1. CHEMICAL ENGINEERING JOURNAL. 421, Number 2 Abstract
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2014
Barbosa, DJ, Serrat R, Mirra S, Quevedo M, Gomez de Barreda E, Avila J, Ferreira LM, Branco PS, Fernandes E, de Bastos ML, Capela JP, Soriano E, Carvalho F.  2014.  The Mixture of ``Ecstasy{''} and Its Metabolites Impairs Mitochondrial Fusion/Fission Equilibrium and Trafficking in Hippocampal Neurons, at In Vivo Relevant Concentrations, JUN. TOXICOLOGICAL SCIENCES. 139, Number 2 Abstract
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Barbosa, DJ, Capela JP, Silva R, Vilas-Boas V, Ferreira LM, Branco PS, Fernandes E, de Bastos ML, Carvalho F.  2014.  The mixture of ``ecstasy{''} and its metabolites is toxic to human SH-SY5Y differentiated cells at in vivo relevant concentrations, FEB. ARCHIVES OF TOXICOLOGY. 88:455-473., Number 2 Abstract
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Sa, S, Gawande MB, Velhinho A, Veiga JP, Bundaleski N, Trigueiro J, Tolstogouzov A, Teodoro OMND, Zboril R, Varma RS, Branco PS.  2014.  Magnetically recyclable magnetite-palladium (Nanocat-Fe-Pd) nanocatalyst for the Buchwald-Hartwig reaction. GREEN CHEMISTRY. 16:3494-3500., Number 7 Abstract
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2013
Vilas-Boasa, V, Silva R, Nunes C, Reis S, Ferreira L, Vieira C, Carvalho F, de Bastos ML, Remiao F.  2013.  Mechanisms of P-gp inhibition and effects on membrane fluidity of a new rifampicin derivative, 1,8-dibenzoyl-rifampicin, JUL 18. TOXICOLOGY LETTERS. 220:259-266., Number 3 Abstract

Purpose: To assess P-glycoprotein (P-gp)-modulation ability and the mechanisms of P-gp inhibition mediated by a new synthetic rifampicin derivative, 1,8-dibenzoyl-rifampicin (DiBenzRif), in an in vitro model of the blood-brain barrier (BBB), RBE4 cells, and in membrane mimetic models (liposomes). Methods: P-gp expression (western blot) and activity {[}rhodamine 123 accumulation studies] were assessed until 72 h of exposure to DiBenzRif. The effects on intracellular ATP levels and on P-gp ATPase activity were studied using luciferin-luciferase bioluminescence assay. Membrane fluidity changes were tracked by steady-state anisotropy measurements. Non-P-gp-related rhodamine 123 accumulation was evaluated using liposomes prepared with the main lipids present in RBE4 cell membranes. Results: A significant increase in intracellular rhodamine 123 content was observed in DiBenzRif-treated cells at all tested time-points. This effect was associated with a significant reduction in ATP intracellular levels, the inhibition of P-gp ATPase activity and a significant increase in membrane fluidity. DiBenzRif also favoured rhodamine 123 accumulation in a liposomal model of RBE4 cells, suggesting that it may be useful in increasing intracellular levels of substances that passively diffuse into the cells. Conclusion: DiBenzRif-induced inhibitory effect on P-gp increases xenobiotic accumulation in BBB cells, which may contribute to the development of therapeutic adjuvants to enhance brain penetration of drugs. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

Gawande, MB, Bonifacio VDB, Varma RS, Nogueira ID, Bundaleski N, Ghumman ACA, Teodoro OMND, Branco PS.  2013.  Magnetically recyclable magnetite-ceria (Nanocat-Fe-Ce) nanocatalyst - applications in multicomponent reactions under benign conditions. GREEN CHEMISTRY. 15:1226-1231., Number 5 Abstract
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2010
Pontes, H, de Pinho PG, Fernandes E, Branco PS, Ferreira LM, Carmo H, Remiao F, Carvalho F, Bastos ML.  2010.  Metabolic interactions between ethanol and MDMA in primary cultured rat hepatocytes, APR 11. TOXICOLOGY. 270:150-157., Number 2-3 Abstract

3,4-Methylenedioxymethamphetamine (MDMA; ecstasy), a drug of abuse commonly consumed at rave parties, is often taken in a polydrug abuse scenario, ethanol being one of the most associated drugs. Both MDMA and ethanol are mainly metabolized in the liver with formation of toxic metabolites. Our working hypothesis is that ethanol can modify the metabolism of MDMA through the cytochrome P450 system, and that this effect may be further potentiated by hyperthermia, a well-known consequence of MDMA abuse. To investigate these putative interactions we used primary rat hepatocyte cultures, which were exposed to 300 mM ethanol, 1.6 mM MDMA and the combination of both, at normothermic (36.5 degrees C) and hyperthermic (40.5 degrees C) conditions. After 24 h, the levels of MDA, HMA and HMMA in the cell culture medium were quantified by GC/MS. In addition, we repeated the same experimental design preceded by 1 h incubation with 0.18 mu M ketoconazole or 150 mu M diallyl sulphide (CYP3A and CYP2E1 inhibitors, respectively), to evaluate the putative role of these isoenzymes in the observed effects. The results obtained showed that ethanol exposure increases the formation of some MDMA metabolites such as HMA (1.8 times increase) and MDA (1.5 times increase). This effect was markedly increased under hyperthermic conditions (HMA, MDA and HMMA formation increased 10,6 and 16 times, respectively) and is mediated, at least partially, by CYP3A and CYP2E1. (C) 2010 Elsevier Ireland Ltd. All rights reserved.